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<record><TEI><teiHeader><fileDesc><titleStmt><title xml:lang="en">Creatine and Its Potential Therapeutic Value for Targeting Cellular Energy Impairment in Neurodegenerative Diseases</title><author><name sortKey="Adhihetty, Peter J" sort="Adhihetty, Peter J" uniqKey="Adhihetty P" first="Peter J." last="Adhihetty">Peter J. Adhihetty</name></author><author><name sortKey="Beal, M Flint" sort="Beal, M Flint" uniqKey="Beal M" first="M. Flint" last="Beal">M. Flint Beal</name></author></titleStmt><publicationStmt><idno type="wicri:source">PMC</idno><idno type="pmid">19005780</idno><idno type="pmc">2886719</idno><idno type="url">http://www.ncbi.nlm.nih.gov/pmc/articles/PMC2886719</idno><idno type="RBID">PMC:2886719</idno><idno type="doi">10.1007/s12017-008-8053-y</idno><date when="2008">2008</date><idno type="wicri:Area/Pmc/Corpus">000201</idno><idno type="wicri:explorRef" wicri:stream="Pmc" wicri:step="Corpus" wicri:corpus="PMC">000201</idno></publicationStmt><sourceDesc><biblStruct><analytic><title xml:lang="en" level="a" type="main">Creatine and Its Potential Therapeutic Value for Targeting Cellular Energy Impairment in Neurodegenerative Diseases</title><author><name sortKey="Adhihetty, Peter J" sort="Adhihetty, Peter J" uniqKey="Adhihetty P" first="Peter J." last="Adhihetty">Peter J. Adhihetty</name></author><author><name sortKey="Beal, M Flint" sort="Beal, M Flint" uniqKey="Beal M" first="M. Flint" last="Beal">M. Flint Beal</name></author></analytic><series><title level="j">Neuromolecular medicine</title><idno type="ISSN">1535-1084</idno><idno type="eISSN">1559-1174</idno><imprint><date when="2008">2008</date></imprint></series></biblStruct></sourceDesc></fileDesc><profileDesc><textClass></textClass></profileDesc></teiHeader><front><div type="abstract" xml:lang="en"><p id="P1">Substantial evidence indicates bioenergetic dysfunction and mitochondrial impairment contribute either directly and/or indirectly to the pathogenesis of numerous neurodegenerative disorders. Treatment paradigms aimed at ameliorating this cellular energy deficit and/or improving mitochondrial function in these neurodegenerative disorders may prove to be useful as a therapeutic intervention. Creatine is a molecule that is produced both endogenously, and acquired exogenously through diet, and is an extremely important molecule that participates in buffering intracellular energy stores. Once creatine is transported into cells, creatine kinase catalyzes the reversible transphosphorylation of creatine via ATP to enhance the phosphocreatine energy pool. Creatine kinase enzymes are located at strategic intracellular sites to couple areas of high energy expenditure to the efficient regeneration of ATP. Thus, the creatinekinase/phosphocreatine system plays an integral role in energy buffering and overall cellular bioenergetics. Originally, exogenous creatine supplementation was widely used only as an ergogenic aid to increase the phosphocreatine pool within muscle to bolster athletic performance. However, the potential therapeutic value of creatine supplementation has recently been investigated with respect to various neurodegenerative disorders that have been associated with bioenergetic deficits as playing a role in disease etiology and/or progression which include; Alzheimer’s, Parkinson’s, amyotrophic lateral sclerosis (ALS), and Huntington’s disease. This review discusses the contribution of mitochondria and bioenergetics to the progression of these neurodegenerative diseases and investigates the potential neuroprotective value of creatine supplementation in each of these neurological diseases. In summary, current literature suggests that exogenous creatine supplementation is most efficacious as a treatment paradigm in Huntington’s and Parkinson’s disease but appears to be less effective for ALS and Alzheimer’s disease.</p></div></front></TEI><pmc article-type="research-article" xml:lang="EN"><pmc-comment>The publisher of this article does not allow downloading of the full text in XML form.</pmc-comment>
<pmc-dir>properties manuscript</pmc-dir>
<front><journal-meta><journal-id journal-id-type="nlm-journal-id">101135365</journal-id><journal-id journal-id-type="pubmed-jr-id">29654</journal-id><journal-id journal-id-type="nlm-ta">Neuromolecular Med</journal-id><journal-title>Neuromolecular medicine</journal-title><issn pub-type="ppub">1535-1084</issn><issn pub-type="epub">1559-1174</issn></journal-meta><article-meta><article-id pub-id-type="pmid">19005780</article-id><article-id pub-id-type="pmc">2886719</article-id><article-id pub-id-type="doi">10.1007/s12017-008-8053-y</article-id><article-id pub-id-type="manuscript">NIHMS196779</article-id><article-categories><subj-group subj-group-type="heading"><subject>Article</subject></subj-group></article-categories><title-group><article-title>Creatine and Its Potential Therapeutic Value for Targeting Cellular Energy Impairment in Neurodegenerative Diseases</article-title></title-group><contrib-group><contrib contrib-type="author"><name><surname>Adhihetty</surname><given-names>Peter J.</given-names></name></contrib><contrib contrib-type="author" corresp="yes"><name><surname>Beal</surname><given-names>M. Flint</given-names></name><email>mfbeal@med.cornell.edu</email></contrib><aff id="A1">Department of Neurology and Neuroscience, Weill Medical College of Cornell University, 525 East 68th Street, New York, NY 10021, USA</aff></contrib-group><pub-date pub-type="nihms-submitted"><day>1</day><month>6</month><year>2010</year></pub-date><pub-date pub-type="epub"><day>13</day><month>11</month><year>2008</year></pub-date><pub-date pub-type="ppub"><year>2008</year></pub-date><pub-date pub-type="pmc-release"><day>16</day><month>6</month><year>2010</year></pub-date><volume>10</volume><issue>4</issue><fpage>275</fpage><lpage>290</lpage><permissions><copyright-statement>© Humana Press Inc. 2008</copyright-statement><copyright-year>2008</copyright-year></permissions><abstract><p id="P1">Substantial evidence indicates bioenergetic dysfunction and mitochondrial impairment contribute either directly and/or indirectly to the pathogenesis of numerous neurodegenerative disorders. Treatment paradigms aimed at ameliorating this cellular energy deficit and/or improving mitochondrial function in these neurodegenerative disorders may prove to be useful as a therapeutic intervention. Creatine is a molecule that is produced both endogenously, and acquired exogenously through diet, and is an extremely important molecule that participates in buffering intracellular energy stores. Once creatine is transported into cells, creatine kinase catalyzes the reversible transphosphorylation of creatine via ATP to enhance the phosphocreatine energy pool. Creatine kinase enzymes are located at strategic intracellular sites to couple areas of high energy expenditure to the efficient regeneration of ATP. Thus, the creatinekinase/phosphocreatine system plays an integral role in energy buffering and overall cellular bioenergetics. Originally, exogenous creatine supplementation was widely used only as an ergogenic aid to increase the phosphocreatine pool within muscle to bolster athletic performance. However, the potential therapeutic value of creatine supplementation has recently been investigated with respect to various neurodegenerative disorders that have been associated with bioenergetic deficits as playing a role in disease etiology and/or progression which include; Alzheimer’s, Parkinson’s, amyotrophic lateral sclerosis (ALS), and Huntington’s disease. This review discusses the contribution of mitochondria and bioenergetics to the progression of these neurodegenerative diseases and investigates the potential neuroprotective value of creatine supplementation in each of these neurological diseases. In summary, current literature suggests that exogenous creatine supplementation is most efficacious as a treatment paradigm in Huntington’s and Parkinson’s disease but appears to be less effective for ALS and Alzheimer’s disease.</p></abstract><kwd-group><kwd>Alzheimer’s</kwd><kwd>Huntington’s</kwd><kwd>Parkinson’s</kwd><kwd>Amyotrophic lateral sclerosis</kwd><kwd>Mitochondria</kwd><kwd>Apoptosis</kwd><kwd>Bioenergetics</kwd><kwd>Reactive oxygen species</kwd></kwd-group><contract-num rid="AG1">P01 AG014930-09
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